Transcriptional regulation of elsinochrome phytotoxin biosynthesis by an EfSTE12 activator in the citrus scab pathogen Elsinoë fawcettii

Abstract

Elsinochrome (ESC), produced by the citrus pathogen Elsinoë fawcettii, is a nonhost-selective, light-dependent, polyketide-derived phytotoxin and plays a crucial role for full virulence. The biosynthesis of ESC is regulated by a wide array of environmental stimuli and is primarily governed by the pathway-specific TSF1 transcription regulator whose coding gene is clustered with the EfPKS1 gene encoding a polyketide synthase and other biosynthetic genes in the genome. In this report, an EfSTE12 gene, encoding a polypeptide resembling the yeast STE12 transcription factor, was cloned and characterized to play a role, independent of TSF1, for ESC production in E. fawcettii. The loss-of-function mutant, specifically disrupted at the EfSTE12 locus, displays reduced ESC accumulation, elevated activities for pectinase and proteolytic enzymes but unaltered in conidiation and fungal pathogenicity. Impairment of the EfSTE12 gene decreased the abundance of the EfPKS1 but not the TSF1 gene transcript. In contrast, expression of the EfSTE12 gene appears normal in the EfPKS1 or TSF1 disruptants. The results indicate that EfSTE12 is functioning for ESC biosynthesis by directly activating the biosynthetic genes without regulating the pathway-specific TSF1 regulator. The defective phenotypes were fully reverted when a functional copy of EfSTE12 was re-introduced into the disrupted mutant. A hypothetical model underlying intertwined regulatory pathways via TSF1, EfSTE12, and other potent transcriptional activators led to the ESC biosynthesis and conidiation is described.